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ABSTRACT Oceanic transform faults are a significant component of the global plate boundary system and are well known for generating fewer and smaller earthquakes than expected. Detailed studies at a handful of sites support the hypothesis that an abundance of creeping segments is responsible for most of the observed deficiency of earthquakes on those faults. We test this hypothesis on a global scale. We relocate Mw ≥5 earthquakes on 138 oceanic transform faults around the world and identify creeping segments on these faults. We demonstrate that creeping segments occur on almost all oceanic transform faults, which could explain their deficiency of earthquakes. We also find that most of the creeping segments are not associated with any large-scale geological structure such as a fault step-over, indicating that along-strike variation of fault zone properties may be the main reason for their existence. 

Abstract Earthquake clustering can be promoted by local, regional, and remote triggering. The interaction between faults by static and dynamic stress transfer has received much attention. However, the role of quasi‐static stress interaction mediated by viscoelastic flow is still poorly understood. Here, we investigate whether the tight synchronization of moment‐magnitude 6 earthquakes every about 6 years on distant asperities in the Gofar‐Discovery fault system of the East Pacific Rise may be caused by mechanical coupling within the lithosphere‐asthenosphere system. We build a three‐dimensional numerical model of seismic cycles in the framework of rate‐ and state‐dependent friction with a brittle layer overlaying a viscoelastic mantle with nonlinear rheology to simulate earthquake cycles on separate asperities. The brittle section of the West Gofar fault consists of two frictionally unstable 20 km‐long by 5 km‐wide asperities separated by a velocity‐strengthening barrier, consistent with seismic observations, allowing stress transfer by afterslip and viscoelastic relaxation. We find that viscoelastic stress transfer can promote the synchronization of earthquakes. Even if the asperities are separated by as far as 30 km, synchronization is still possible for a viscosity of the underlying mantle of 10¹⁷ Pa s, which can be attained by dislocation creep or transient creep during the postseismic period. Considering the similarities in tectonic and structural settings, viscoelastic stress transfer and earthquake synchronization may also occur at 15’20 (Mid‐Atlantic Ridge), George V (Southeast Indian Ridge), Menard and Heezen transform fault (Pacific‐Antarctic Ridge). 

Abstract Synchronization behavior of large earthquakes (rupture of nearby faults close in time for many cycles) has been reported in many fault systems. The general idea is that the faults in the system have similar repeating intervals and are positively coupled through stress interaction. However, many details of such synchronization remain unknown. Here, we built a numerical model in the framework of rate‐and‐state friction to simulate earthquake cycles on the west Gofar fault, East Pacific Rise. Our model consists of two seismic patches separated by a barrier patch, which are constrained by seismic observations. We varied the parameters in the barrier to understand its role on earthquake synchronization. First, we found that when the barrier is relatively weak, synchronization can be achieved by afterslip or post‐seismic creep in the barrier patch. Second, static stress transfer can lead to synchronization, opposite to the suggestion by Scholz (2010,https://doi.org/10.1785/0120090309), which was based on results from a spring‐slider model using rate‐and‐state friction. Third, the width of the barrier is more important than its strength. When the barrier is narrow enough (no more than half the width of the seismic patch in our model), the system can achieve synchronization even with a very strong barrier. Fourth, for certain simulations, the interaction between the two seismic patches promotes partial rupture in the seismic patches and leads to complex behavior: the system switches from synchronized to unsynchronized over 10–20 cycles. 

Plants balance their competing requirements for growth and stress tolerance via a sophisticated regulatory circuitry that controls responses to the external environments. We have identified a plant-specific gene, COST1 ( constitutively stressed 1 ), that is required for normal plant growth but negatively regulates drought resistance by influencing the autophagy pathway. An Arabidopsis thaliana cost1 mutant has decreased growth and increased drought tolerance, together with constitutive autophagy and increased expression of drought-response genes, while overexpression of COST1 confers drought hypersensitivity and reduced autophagy. The COST1 protein is degraded upon plant dehydration, and this degradation is reduced upon treatment with inhibitors of the 26S proteasome or autophagy pathways. The drought resistance of a cost1 mutant is dependent on an active autophagy pathway, but independent of other known drought signaling pathways, indicating that COST1 acts through regulation of autophagy. In addition, COST1 colocalizes to autophagosomes with the autophagosome marker ATG8e and the autophagy adaptor NBR1, and affects the level of ATG8e protein through physical interaction with ATG8e, indicating a pivotal role in direct regulation of autophagy. We propose a model in which COST1 represses autophagy under optimal conditions, thus allowing plant growth. Under drought, COST1 is degraded, enabling activation of autophagy and suppression of growth to enhance drought tolerance. Our research places COST1 as an important regulator controlling the balance between growth and stress responses via the direct regulation of autophagy.